Aim. To identify the factors protecting Abeta-positive subjects with normal cognition (NC) or mild cognitive impairment (MCI) from conversion to Alzheimer’s disease (AD). Methods. Subjects with MCI in the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database, with baseline data for neuropsychological tests, brain beta amyloid (Abeta), magnetic resonance imaging (MRI), APOE genotyping, and 18F-FDG-PET (FDG), were included for analysis. Results. Elevated brain amyloid was associated with a higher risk of conversion from MCI to AD (41.5%) relative to Abeta levels of <1.231 (5.5%) but was not associated with conversion from NC to AD (0.0 vs. 1.4%). In the multivariate Cox regression analyses, elevated Abeta increased the risk of AD, while higher whole-brain cerebral glucose metabolism (CGM) assessed by FDG decreased the risk of AD in subjects with the same amount of Abeta. Even in the patients with heavily elevated brain amyloid, those with had a lower risk of AD. ApoE4 carrier status did not influence the protective effect. Conclusion. Higher average CGM based on FDG modified the progression to AD, indicating a protective function. The results suggest that the inclusion of this CGM measured by FDG would enrich clinical trial design and that increasing CGM along with the use of anti-Abeta agents might be a potential prevention strategy for AD.

中文翻译：

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保护因素调节阿尔茨海默病中 β 淀粉样蛋白的风险

瞄准。确定保护具有正常认知 (NC) 或轻度认知障碍 (MCI) 的 Abeta 阳性受试者免于转化为阿尔茨海默病 (AD) 的因素。方法。包括阿尔茨海默病神经影像学倡议 (ADNI) 数据库中具有 MCI 的受试者，以及神经心理学测试、脑 β 淀粉样蛋白 (Abeta)、磁共振成像 (MRI)、APOE 基因分型和 18F-FDG-PET (FDG) 的基线数据进行分析。结果. 相对于 <1.231 (5.5%) 的 Abeta 水平，升高的脑淀粉样蛋白与从 MCI 转化为 AD 的风险较高 (41.5%) 相关，但与从 NC 转化为 AD 无关（0.0 对 1.4%）。在多变量 Cox 回归分析中，升高的 Abeta 增加了 AD 的风险，而通过 FDG 评估的更高的全脑脑葡萄糖代谢 (CGM) 降低了具有相同 Abeta 量的受试者患 AD 的风险。即使在脑淀粉样蛋白严重升高的患者中，患 AD 的风险较低。ApoE4携带状态不影响保护效果。结论。基于 FDG 的较高平均 CGM 改变了向 AD 的进展，表明具有保护功能。结果表明，包含 FDG 测量的这种 CGM 将丰富临床试验设计，并且增加 CGM 以及使用抗 Abeta 药物可能是 AD 的潜在预防策略。